This research is intended to test the two components of the following hypothesis: 1) Mineralocorticoid hypertension is initiated by an action of this steroid on the brain. 2) This action causes the release of a humoral factor that increases membrane permeability to sodium in peripheral tissues. This peripheral action will be evaluated by measuring passive sodium flux in lymphocytes. The central origin of a humoral agent that increases this sodium flux will be tested by determining whether the change in sodium flux occurs when DOCA is administered to rats that have been pretreated intracerebroventricular (IVT) with the neurotoxin, 6-hydroxydopamine. Studies of passive sodium flux in lymphocytes will also be carried out in rats receiving chronic IVT infusions of minute amounts of desoxycorticosterone (DOC). In vitro and in vivo studies of the influence of DOC on passive sodium flux in lymphocytes will be performed in pig plasma. This study will permit a characterization of the direct and indirect (secondary to the postulated humoral factor of central origin) actions of the steroid on the lymphocyte membrane. These new insights into the mechanism of this form of hypertension should permit the identification of specific target sites for therapeutic interventions.